| First Author | Wild R | Year | 2004 |
| Journal | Breast Cancer Res Treat | Volume | 85 |
| Issue | 2 | Pages | 161-71 |
| PubMed ID | 15111774 | Mgi Jnum | J:90175 |
| Mgi Id | MGI:3042655 | Doi | 10.1023/B:BREA.0000025407.02896.ec |
| Citation | Wild R, et al. (2004) VEGF-DT385 Toxin Conjugate Inhibits Mammary Adenocarcinoma Development in a Transgenic Mouse Model of Spontaneous Tumorigenesis. Breast Cancer Res Treat 85(2):161-71 |
| abstractText | Previous experiments have shown that a vascular endothelial growth factor (VEGF)-DT385 toxin conjugate inhibits endothelial cell proliferation, angiogenesis and solid tumor growth in a xenotransplant model system. Here, we report that VEGF-DT385 toxin conjugate effectively inhibits spontaneous tumorigenesis. The C3(1)/SV40 TAg transgenic mouse model of mammary gland carcinogenesis was used to determine the effectiveness of VEGF-DT385 toxin conjugate in delaying the onset of disease and the development of solid tumors. Animals were treated daily with conjugate for a period of 7 days. Therapy was initiated at week 14 of development before any visible adenocarcinomas were evident. Treatment of mice with VEGF-DT385 toxin conjugate significantly delayed the onset of tumorigenesis and inhibited solid tumor growth by more than 92%. Furthermore, conjugate treated animals showed less than twice the number of tumor nodules when compared to control mice. Finally, this vascular targeting agent significantly increased survival time of animals by 5 weeks. VEGF-DT385 toxin conjugate resulted in temporary weight loss and no long-lasting toxicity was seen. More importantly, using this established tumor model, VEGF-DT385 toxin conjugate appeared to be as effective as a similar treatment schedule with recombinant human endostatin. Our results suggest that VEGF-DT385 toxin conjugate is a potent inhibitor of mammary adenocarcinoma growth and might be useful in breast cancer therapy. |
